翼状胬肉切除联合自体角膜缘干细胞移植术治疗翼状胬肉临床观察

目的观察翼状胬肉切除联合自体角膜缘干细胞移植术治疗翼状胬肉的疗效。方法采用翼状胬肉切除联合自体角膜缘干细胞移植术方法治疗翼状胬肉【】50例(52只眼)观察术后角膜情况进行术前术后对比,并随访半年。结果 50例(52只眼)手术中、术后无严重并发症,随访半年,只有1例复发。结论翼状胬肉联合自体角膜缘干细胞移植术,疗效满意,大大降低术后复发率。     

Pilot study of transepithelial， very high fluence accelerated corneal collagen cross-linking in primary keratoconus

Objective Evaluate the safety and effectiveness of transepithelial, very high fluence accelerated corneal collagen cross-linking （A-CXL） in primary keratoconus. Methods Self-control study. Thirteen primary keratoconus eyes of 13 patients were treated with transepthelial, very high fluence A-CXL with a UVA intensity of 45 mW/cm2, an irradiation time of 2 min 40 s, and a total energy of 7.2 J/cm2. Routine ophthalmologic examination, UCVA, BCVA, refractive error, corneal keratometry, anterior and posterior elevation （AE and PE）, index of vertical asymmetry （IVA）, minimum corneal thickness （CT）, compensated intraocular pressure （IOPcc）, endothelial cell density （ECD） were evaluated pre-operatively and 7-day, 1-month, 3-month, 6-month, 12-month post-operatively. Results The UCVA （F=6.111, P＜0.01） and BCVA （F=9.734, P＜0.01） showed a statistically significant improvement by 12-month post-operatively. The decrease in spherical lens （F=5.871, P＜0.05）, steeper K-value （F=19.651, P＜0.05）, Kmax （F=3.253, P＜0.05）, AE （F=23.958, P＜0.01）, PE （F=20.832, P＜0.01） and IVA （F=4.068, P＜0.05） were statistically significant. CT （F=4.180, P＞0.05）, ECD （F=1.812, P＞0.05） and IOPcc （F=0.332, P＞0.05） were without significant change. Conclusion Transepithelial, very high fluence A-CXL is safe and effective in treating primary keratoconus.     

A comparative study on endothelial cell loss in nanophthalmic eyes undergoing cataract surgery by phacoemulsification

Purpose:The purpose of this study is to compare the endothelial cell loss (ECL) in nanophthalmic eyes and age-matched controls undergoing cataract surgery by phacoemulsification and also to identify the risk factors influencing the endothelial cell density (ECD). This was a prospective comparative interventional case series.Methods:We enrolled 19 nanophthalmic eyes (study group) and 42 age-matched cataract controls (control group) undergoing phacoemulsification after meeting the inclusion criteria. Ocular parameters like best-corrected visual acuity, intraocular pressure, pachymetry, specular microscopy, and slit lamp findings were noted preoperatively and at month 1 and 3 postsurgery. All nanophthalmic eyes underwent cataract surgery with concomitant prophylactic posterior sclerostomy.Results:The median percentage endothelial loss in nanophthalmic eyes was 4.0 (IQR 0–23.5), 7.4 (IQR 1.0–-22.4) at 1 and 3 months postoperatively compared to 6.3 (IQR 1.7–14.1) and 6.4 (IQR 2.6–-12.1) in age controlled normal eyes (P = 0.94, P = 0.46, respectively). Linear regression analysis showed increasing age as the only variable influencing the percentage decrease in corneal ECD in the study group (P = 0.001). Nanophthalmic eyes with ACD <2.5 mm had a significantly greater reduction in ECD at 3 months postcataract surgery compared to baseline (P = 0.039). Visual outcomes and IOP reduction in the study group with ACD >2.5 mm were significantly better postcataract surgery (P = 0.02 and P = 0.002, respectively).Conclusion:The percentage of ECL in nanophthalmic eyes undergoing phacoemulsification is equivalent to normal eyes. However, in the nanophthamic eyes with AC depth <2.5 mm, the percentage cell loss was significantly higher warranting the need for extensive intraoperative care. Increasing age was found to be the only significant risk factor influencing the ECD in short eyes.     

Intracorneal scleral patch supported cyanoacrylate application for corneal perforations secondary to rheumatoid arthritis

Purpose:To describe a new technique of intracorneal scleral patch (ICSP) supported cyanoacrylate tissue adhesive (CTA) application in corneal perforations, greater than 3.0 mm secondary to rheumatoid arthritis (RA).Methods:This Prospective, non-randomized, non-comparative, interventional series included 14 eyes (14 patients). All patients had corneal perforations sized 3.5 to 4.5 mm due to RA, which were treated with ICSP supported CTA application. A partial thickness scleral patch 1.0 mm larger than diameter of corneal perforation was prepared. A lamellar corneal pocket 0.5 mm all around the corneal perforation was created. The partial thickness scleral patch was placed in the corneal perforation site and the edge was fitted into the lamellar intracorneal pocket. A minimum quantity of CTA was applied on the scleral patch to seal the perforation.Results:The corneal perforations healed in 14 eyes (100%) in a mean 7.71 ± 1.14 (range, 6–9) weeks. One eye (7.14%) had inadvertent extrusion of ICSP due to premature removal of CTA but, Seidel''s test was negative, and the corneal epithelial defect healed with BCL alone. One eye each (7.14%) developed steroid induced cataract and glaucoma. None of eyes developed infective keratitis, re-opening of corneal perforation (necessitating repeat procedure) or enlargement of corneal perforation requiring penetrating keratoplasty (PKP).Conclusion:ICSP supported CTA application is a successful alternative option to emergency PKP in treating corneal perforations sized 3.5 to 4.5 mm with associated RA.     

The molecular basis of neurotrophic keratopathy: Diagnostic and therapeutic implications. A review

Neurotrophic keratopathy (NK) is a degenerative corneal disease produced by different factors, including infection, trauma, and neurogenesis, that lead to trigeminal nerve damage and impaired corneal sensitivity. Extensive epithelial breakdown, impaired corneal epithelial healing and corneal ulceration, stromal melting, and perforation are main NK features. The proliferation of the corneal epithelium is endogenously regulated by a balance between adrenergic cAMP-dependent and cholinergic cGMP-dependent pathways. A careful balance of epitheliotropic neuromediators and neurotrophic factors expressed by corneal nerves and epithelial cells, respectively, is required to maintain corneal homeostasis. Even in its early stages, NK can cause reduced vision secondary to epithelial disturbance. Diagnosing NK is challenging, requiring the acquisition of a thorough clinical history and a comprehensive neurological and ophthalmic examination. Following suspicion of a clinical NK diagnosis, corneal sensitivity must be assessed qualitatively with the wisp of the cotton-tipped applicator and quantitatively through Cochet-Bonnet esthesiometry (CBE). A myriad of therapies is used for NK, and new, more specific modalities are being developed and investigated. Medical treatment with topical recombinant human nerve growth factor and surgical treatment through corneal neurotization are promising therapies aiming to target NK pathophysiology. Coexistent ocular surface disorders must be managed concomitantly to improve its prognosis. This review describes the up-to-date knowledge of the molecular basis regarding the pathogenesis of NK, and the novel target-specific therapeutic approaches based on this molecular mechanism.     

The role of nitric oxide in ocular surface physiology and pathophysiology

Nitric oxide (NO) has a wide array of biological functions including the regulation of vascular tone, neurotransmission, immunomodulation, stimulation of proinflammatory cytokine expression and antimicrobial action. These functions may depend on the type of isoform that is responsible for the synthesis of NO. NO is found in various ocular tissues playing a pivotal role in physiological mechanisms, namely regulating vascular tone in the uvea, retinal blood circulation, aqueous humor dynamics, neurotransmission and phototransduction in retinal layers. Unregulated production of NO in ocular tissues may result in production of toxic superoxide free radicals that participate in ocular diseases such as endotoxin-induced uveitis, ischemic proliferative retinopathy and neurotoxicity of optic nerve head in glaucoma. However, the role of NO on the ocular surface in mediating physiology and pathophysiological processes is not fully understood. Moreover, methods used to measure levels of NO in the biological samples of the ocular surface are not well established due to its rapid oxidation. The purpose of this review is to highlight the role of NO in the physiology and pathophysiology of ocular surface and propose suitable techniques to measure NO levels in ocular surface tissues and tears. This will improve the understanding of NO's role in ocular surface biology and the development of new NO-based therapies to treat various ocular surface diseases. Further, this review summarizes the biochemistry underpinning NO's antimicrobial action.     

Corneal lymphangiogenesis in dry eye disease is regulated by substance P/neurokinin-1 receptor system through controlling expression of vascular endothelial growth factor receptor 3

PurposeTo evaluate the role of substance P (SP)/neurokinin-1 receptor (NK1R) system in the regulation of pathologic corneal lymphangiogenesis in dry eye disease (DED).MethodsImmunocytochemistry, angiogenesis assay, and Western blot analysis of human dermal lymphatic endothelial cells (HDLECs) were conducted to assess the involvement of SP/NK1R system in lymphangiogenesis. DED was induced in wild-type C57BL/6 J mice using controlled-environment chamber without scopolamine. Immunohistochemistry, corneal fluorescein staining, and phenol red thread test were used to evaluate the effect of SP signaling blockade in the corneal lymphangiogenesis. The expression of lymphangiogenic factors in the corneal and conjunctival tissues of DED mouse model was quantified by real-time polymerase chain reaction.ResultsNK1R expression and pro-lymphangiogenic property of SP/NK1R system in HDLECs were confirmed by Western blot analysis and angiogenesis assay. Blockade of SP signaling with L733,060, an antagonist of NK1R, or NK1R-targeted siRNA significantly inhibited lymphangiogenesis and expression of vascular endothelial growth factor (VEGF) receptor 3 stimulated by SP in HDLECs. NK1R antagonist also suppressed pathological corneal lymphangiogenesis and ameliorated the clinical signs of dry eye in vivo. Furthermore, NK1R antagonist effectively suppressed the lymphangiogenic factors, including VEGF-C, VEGF-D, and VEGF receptor 3 in the corneal and conjunctival tissues of DED.ConclusionsSP/NK1R system promotes lymphangiogenesis in vitro and NK1R antagonism suppresses pathologic corneal lymphangiogenesis in DED in vivo.     

Ciliogenesis and autophagy are coordinately regulated by EphA2 in the cornea to maintain proper epithelial architecture

PurposeTo understand the relationship between ciliogenesis and autophagy in the corneal epithelium.MethodssiRNAs for EphA2 or PLD1 were used to inhibit protein expression in vitro. Morpholino-anti-EphA2 was used to knockdown EphA2 in Xenopus skin. An EphA2 knockout mouse was used to conduct loss of function studies. Autophagic vacuoles were visualized by contrast light microscopy. Autophagy flux, was measured by LC3 turnover and p62 protein levels. Immunostaining and confocal microscopy were conducted to visualize cilia in cultured cells and in vivo.ResultsLoss of EphA2 (i) increased corneal epithelial thickness by elevating proliferative potential in wing cells, (ii) reduced the number of ciliated cells, (iii) increased large hollow vacuoles, that could be rescued by BafA1; (iv) inhibited autophagy flux and (v) increased GFP-LC3 puncta in the mouse corneal epithelium. This indicated a role for EphA2 in stratified epithelial assembly via regulation of proliferation as well as a positive role in both ciliogenesis and end-stage autophagy. Inhibition of PLD1, an EphA2 interacting protein that is a critical regulator of end-stage autophagy, reversed the accumulation of vacuoles, and the reduction in the number of ciliated cells due to EphA2 depletion, suggesting EphA2 regulation of both end-stage autophagy and ciliogenesis via PLD1. PLD1 mediated rescue of ciliogenesis by EphA2 depletion was blocked by BafA1, placing autophagy between EphA2 signaling and regulation of ciliogenesis.ConclusionOur findings demonstrate a novel role for EphA2 in regulating both autophagy and ciliogenesis, processes that are essential for proper corneal epithelial homeostasis.     

Mycobacterium fortuitum keratitis

We report a case of mycobacterial keratitis characterized by apparently spontaneous onset, delayed diagnosis, and eventually necessitating evisceration inspite of systemic antibiotics and repeated corneal grafts.